Search PubMed⌕ Search

Biomedical subjects

M Nagano

Publications and source records attributed to M Nagano.

At least 397 records · Page 22Linked to original sources
PubMedDate not supplied

Chylous cyst of the mesentery: US and CT diagnosis.

We report a case of mesenteric chylous cyst diagnosed preoperatively by ultrasonography (US) and computed tomography (CT). Both demonstrated a unilocular cystic mass with a fluid-fluid level. The CT number of the two components indicated fat density and water density and with shaking or positional changes, the contents displayed miscibility. The tumor changed its position during hospitalization. Both features are considered to be quite diagnostic of this condition.

Chyle↗
PubMedDate not supplied

Myocardial contractility and ventricular myosin isoenzymes as influenced by cardiac hypertrophy and its regression.

Changes in myocardial contractility and ventricular myosin isoenzymes were examined during pressure-overloaded cardiac hypertrophy in rats. Effects of regression of cardiac hypertrophy were also examined. Cardiac hypertrophy was induced by abdominal aortic constriction in 7-week-old male Wistar rats. Regression of cardiac hypertrophy was obtained by opening the aortic band. Myocardial contractility was estimated by measuring isometrically developed tension and maximum rate of tension rise (+dT/dtmax) in isolated left-ventricular papillary muscles perfused with Tyrode solution (32 degrees C, pH 7.4, bubbled with 95% O2.5% CO2, stimulation frequency: 0.2 Hz). Left-ventricular myosin isoenzymes were separated by pyrophosphate gel electrophoresis and the isoenzyme pattern was determined by densitometry. Isometrically developed tension (T) in hypertrophic myocardium remained unchanged, but +/-dT/dtmax decreased as compared with hearts of normal rats. Decreased +/-dT/dtmax recovered near to the level in normal rats by regression of cardiac hypertrophy. Left-ventricular myosin isoenzyme pattern shifted towards VM-3 in hypertrophied myocardium and shifted again toward VM-1 by regression of cardiac hypertrophy. In conclusion, myocardial contractility and ventricular myosin isoenzymes were changed in pressure-overloaded hypertrophy in rats and these changes were reversible to a normal level by regression of cardiac hypertrophy.

Animals↗
PubMedDate not supplied

Early proliferative changes in hearts of hypertensive Goldblatt rats: an immunohistochemical and flow-cytometrical study.

Hyperplasia of myocytes in cardiac adaptation is a rare event in the mammalian cardiac muscle. Recent findings support the concept that proliferation of myocytes in the adult mammalian heart may be induced after a prolonged increase in pressure load on the myocardium. To determine whether short-term hypertension leads to hyperplasia of myocyte nuclei in the rat heart renal hypertension was produced in 12 Wistar rats. As soon as hypertension occurred, bromodeoxyuridine (BrdU) (50 mg/kg/day) was injected intraperitoneally on three subsequent days. Twelve sham-operated rats served as controls. After 3 days, the left cardiac ventricle was excised and double-staining with anti-BrdU antibody and propidium iodide was performed to determine the phase of cell-cycle of the BrdU-positive cells by flow-cytometry. Immunohistochemical double-staining with desmin, smooth muscle actin, vimentin, and BrdU was done to classify the BrdU-positive cells. Most of the BrdU-positive cells were in the G0/G1-phase of the cell-cycle, suggesting cell proliferation or DNA-repair have taken place; polyploidy was not observed. In the hypertensive group (4.62% +/- 2.36) significantly more cells incorporated BrdU than in the control group (1.46% +/- 0.96). Immunohistochemically, the majority of the BrdU-positive cells consisted of fibrocytes, smooth muscle cells, and endothelial cells. Only 0.35% +/- 0.26 of cardiac myocytes in the normotensive group showed positive BrdU-staining compared to 0.48% +/- 0.32 in the hypertensive group. This difference was statistically not significant. This study showed that early after onset of hypertension proliferation of non-myocytes, but not of myocytes occurred. DNA synthesis is limited almost completely to the interstitial cells and does not occur in any significant extent in cardiac myocytes. In conclusion, hyperplasia of cardiac myocytes is not observed at early stages of hypertension, but it may develop at a late stage of cardiac adaptation.

Actins↗
PubMedDate not supplied

Effects of physical training on the myocardium of streptozotocin-induced diabetic rats.

Effects of endurance swimming training on myocardial contractility and left ventricular myosin isoenzymes were examined in diabetic rats. A diabetic condition was induced in 15-week-old male Wistar rats, by intravenous injection of streptozotocin (50 mg/kg). Swimming training was carried out for five to six weeks (90 min/day, 6 days/week). In order to estimate myocardial contractility, the isometric developed tension of the isolated left ventricular papillary muscle was measured. Myosin isoenzymes were obtained by pyrophosphate gel electrophoresis. Fasting blood glucose of the trained group was significantly lower than that of the sedentary group (sedentary vs. trained = 409.6 +/- 25.9 vs. 266.3 +/- 20.5 mg/dl, p less than 0.001). There was no significant difference in isometric developed tension (T) between the two groups, and the dT/dtmax of the trained group showed a tendency to increase (sedentary vs. trained, T: 2.8 +/- 0.8 vs. 2.9 +/- 0.8 g/mm2, dT/dtmax: 23.1 +/- 3.6 vs. 26.2 +/- 3.5 g/mm2.s, p less than 0.1). Myocardial mechanical responses to isoproterenol and dibutyryl cAMP were increased in the trained group. Left ventricular myosin isoenzyme pattern was shifted towards VM-1 by endurance swimming (sedentary vs. trained, VM-1: 5.6 +/- 4.5 vs. 19.6 +/- 8.8%, p less than 0.001, VM-3: 75.1 +/- 10.0 vs. 54.9 +/- 14.7%, p less than 0.001). These results indicate that endurance swimming can improve disordered glucose metabolism and also influence myocardial contractility, myocardial catecholamine responsiveness, and energetics in myocardial contraction.

Animals↗
PubMedDate not supplied

Mechanical catecholamine responsiveness and myosin isoenzyme pattern of pressure-overloaded rat ventricular myocardium.

Pressure-overloaded cardiac hypertrophy was induced by abdominal aortic constriction in 10-week-old male Wistar rats. 24-26 weeks after aortic constriction, the hearts were excised and a myocardial mechanical study was performed using isolated left ventricular papillary muscles. There was no significant difference in isometric developed tension (T) between sham-operated control and aortic constriction (AC) rats (control vs AC rats = 2.9 +/- 0.6 vs 2.7 +/- 0.7 g/mm2). dT/dtmax of AC rats, on the other hand, was significantly lower than that of controls (controls vs AC rats = 32.8 +/- 7.5 vs 26.3 +/- 6.1 g/mm2s, p less than 0.05). Myocardial mechanical responses to isoproterenol (10(-7) mol/l) were depressed in the group with aortic constriction compared with the control group (delta T: 18.5 +/- 6.7 vs 12.1 +/- 4.9%, p less than 0.05, delta dT/dt: 25.2 +/- 6.2 vs 17.5 +/- 5.8%, p less than 0.02). Responses of the parameters to dibutyryl cyclic AMP (10(-5) mol/l) were also smaller in the AC group than in the control group (delta T: 18.0 +/- 5.6 vs 13.3 +/- 4.0%, p less than 0.05, delta dT/dt: 20.4 +/- 6.9 vs 14.7 +/- 4.1%, p less than 0.05). Left ventricular myosin isoenzyme pattern, revealed by pyrophosphate gel electrophoresis, shifted towards VM-3 under pressure overload. The present study demonstrates that post-membrane processes may be mainly responsible for the decreased myocardial mechanical catecholamine responsiveness in pressure-overloaded cardiac hypertrophy.

Animals↗
PubMedDate not supplied

Unilateral pulmonary edema following acute subglottic edema.

Presented here is a case of unilateral pulmonary edema following acute subglottic edema after removal of an endotracheal tube. A 3-year-old boy, diagnosed as having nondiphtheric croup and pectus excavatum deformity, was scheduled for repair of a cleft lip. No complication occurred during the operation. After removal of the endotracheal tube, he showed dyspnea and cyanosis and was later found to have acute subglottic edema. After reintubation of the trachea, frothy pink fluid was discharged from the tube, and chest roentgenogram showed a right-sided alveolar infiltrate. Many factors may cause unilateral pulmonary edema, but it is suggested that acute subglottic edema and unilateral bronchial fragility strongly affected this episode.

Acute Disease↗
PubMedDate not supplied

Antenatal diagnosis and surgical management of congenital cystic adenomatoid malformation of the lung.

We experienced 12 cases of congenital cystic adenomatoid malformation of the lung (CCAM) including 6 cases diagnosed antenatally. They were classified into three groups according to the clinical manifestations. Group A was associated with hydrops fetalis (n = 3), group B presented with respiratory distress symptoms after birth (n = 6), and group C showed no respiratory symptoms (n = 3). All cases of group A were lost because of hydrops and respiratory failure due to pulmonary hypoplasia. Because a compression of the mass is thought to be a cause of hydrops, this group is considered to be a good indication for fetal treatment. All cases of group B showed progressive respiratory symptoms a few days after birth which were successfully treated surgically. In 2 of 3 cases of group C, the lesions decreased in size both antenatally and postnatally. We conclude that serial sonographic evaluations for fetal CCAM are important. If the fetus develops hydrops, fetal surgery is to be considered. If not, however, fetal surgery should not be done, because some lesions can shrink in size, or even disappear, while others can be treated successfully after birth by lobectomy or even segmentectomy.

Cystic Adenomatoid Malformation of Lung, Congenita↗
PubMedDate not supplied

Manganese intoxication during intermittent parenteral nutrition: report of two cases.

BACKGROUND AND METHODS: The administration of trace elements is thought to be needed in patients receiving long-term parenteral nutrition. Recently, manganese intoxication or deposition was documented in such patients. We report two cases of manganese intoxication during intermittent parenteral nutrition including manganese. Manganese had been administered for 4 years at a frequency of one or two times per week in one case and for 5 years at a frequency of one or two times per month in the other case. Both cases showed mild symptoms with headache and dizziness. One case had mild hepatic dysfunction and the other did not. The whole-blood manganese level increased in one case, but not in the other case. T1-weighted magnetic resonance images revealed symmetrical high-intensity areas in basal ganglia and thalamus in both cases. After the administration of manganese was stopped, these symptoms all disappeared and the magnetic resonance images abnormalities gradually improved in both patients. Mild long-term manganese intoxication is thus considered to occur regardless of the frequency of using a manganese supplement. CONCLUSIONS: Patients should be carefully monitored when receiving long-term parenteral nutrition including manganese, even when the manganese dose is small and the frequency of receiving a manganese supplement is low.

Adolescent↗
PubMedDate not supplied

Complications in neonates with short bowel syndrome and long-term parenteral nutrition.

BACKGROUND: Because of advances in parenteral nutrition (PN), the prognosis for patients with short bowel syndrome (SBS) has recently shown great improvement. Even infants with a small bowel measuring only 20 cm either with or without an ileocoecal valve can now survive. However, because of the increased periods of PN, severe complications associated with PN have been observed. PATIENTS AND METHODS: We analyzed 17 patients with SBS treated by long-term PN to investigate the complications of PN, particularly hepatic dysfunction, micronutrient deficiency, and intoxication. RESULTS: Eleven of 17 patients (64.7%) had hepatic dysfunction, mostly cholestasis. The main causes of hepatic dysfunction were loss of enteral feeding and infections. Regarding the complications of the micronutrients, zinc and copper deficiencies have been observed less often because of trace element supplements. However, manganese deposition, especially in the basal ganglia, was recognized in one patient. CONCLUSIONS: We therefore need to pay more attention to these problems when treating this disease in order to improve the overall prognosis significantly.

Cholestasis↗
PubMedDate not supplied

Myocardial metabolism of spontaneously hypertensive rat.

Oxidative phosphorylation of myocardial mitochondria isolated from spontaneously hypertensive rats (SHR) was determined polarographically. The concentrations of high-energy phosphate compounds, the concentrations of intermediate metabolites, and the activities of the enzymes within the metabolic systems of glycolysis, the pentose phosphate (PPh) cycle, and the tricarboxylic acid (TCA) cycle of the myocardium of SHR were determined. The gradual development of cardiac hypertrophy was observed in SHR in comparison with normotensive Wistar rats. There were no significant differences in the function of oxidative phosphorylation of the mitochondria, in concentrations of high-energy phosphate compounds and carbohydrate metabolites, or in activities of glycolytic enzymes between SHR and normotensive Wistar rats.

Adenine Nucleotides↗
PubMedDate not supplied

Role of acetaldehyde in the pathogenesis of alcoholic cardiomyopathy.

Rats given both ethanol and tolbutamide showed decreased oxidative phosphorylation of the myocardial mitochondria as compared with rats given only ethanol. There were no differences in ethanol consumption and blood ethanol levels between the two groups. The concentration of acetaldehyde tended to be higher in rats given both ethanol and tolbutamide than in rats given ethanol alone. It is concluded that acetaldehyde plays a more important role in the production of alcoholic cardiomyopathy than does ethanol itself.

Acetaldehyde↗
PubMedDate not supplied

Influence of long-term arotinolol treatment on myocardial mechanics and ventricular myosin isoenzymes in spontaneously hypertensive rats.

Alterations in myocardial mechanics and left ventricular myosin isoenzymes by long-term treatment of hypertension with arotinolol were examined in spontaneously hypertensive rats. Approximately 20 mg/kg/day arotinolol was administered to 22-week-old male spontaneously hypertensive rats for 8-10 weeks. There was no significant difference in systolic blood pressure between arotinolol-treated and untreated rats. However, ventricular weight tended to decrease in the arotinolol-treated group, although not significantly. There were no significant differences in isometric developed tension and dT/dtmax of isolated left ventricular papillary muscles between the arotinolol-treated and untreated groups. The left ventricular myosin isoenzyme pattern, on the other hand, obtained by pyrophosphate gel electrophoresis, showed a significant shift toward VM-1 as a result of long-term arotinolol treatment.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Metabolic effect of pH on myocardium of heart-lung preparation.

Cardiac performance and metabolism of heart-lung preparation of rat were studied with acid, normal, and alkali perfusions. Cardiac output, glucose uptake, and myocardial content of lactate, malate, glycerophosphate, and CP were increased in alkali and decreased in acid perfusion of 20 min. On the other hand, when pH of the perfusate was abruptly changed, CP and ATP were decreased independent of the performance. FDP was high and PEP was low in acute acidifying experiments. From these findings it is concluded that cardiac performance and carbohydrate metabolism are accelerated in alkali and depressed in acid perfusion, and that myocardial metabolism could be affected by pH not only secondary to the change of performance but also by itself.

Adenine Nucleotides↗
PubMedDate not supplied

Effects of bunazosin on plasma glucose levels in hypertensive diabetic patients.

Twenty-nine hypertensive diabetic patients received 1.5 to 4.0 mg of bunazosin daily for three months. Both systolic and diastolic blood pressures were significantly reduced by the bunazosin treatment, while heart rate was unchanged. No significant changes were noted in fasting plasma glucose levels or in levels of hemoglobin A1c. Serum lipid levels remained unchanged during treatment. It is concluded that bunazosin does not adversely affect glucose metabolism or increase serum lipid levels in hypertensive diabetic patients.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Effects of the angiotensin II receptor antagonist, TCV-116, on blood pressure and the renin-angiotensin system in healthy subjects.

TCV-116 is a new, nonpeptide, angiotensin II type-1 receptor antagonist that acts as a specific inhibitor of the renin-angiotensin system. In this study, 36 healthy male volunteers were administered single and repeated oral doses of TCV-116 to investigate its effects on blood pressure and heart rate, and to evaluate the safety and pharmacokinetics of the drug. At single doses of 2.5 mg and greater, TCV-116 significantly lowered blood pressure even in normotensive subjects. This hypotensive effect was maintained during repeated administration on a once-daily regimen over an 8-day period. Serum concentration of M-1, an active metabolite of TCV-116, increased in a dose-dependent manner, reaching a peak 3 to 4 hours after administration. An amount of M-1 equivalent to approximately 10% of the administered dose of TCV-116 was excreted in the urine during the first 24 hours following administration. No accumulation of M-1 was observed in subjects receiving repeated administration of TCV-116. No adverse effects were observed except for mild headache in three subjects. These results suggest that the renin-angiotensin system plays a role in the regulation of blood pressure, even in normotensive subjects, and that TCV-116 may prove to be useful in the treatment of hypertension.

Adult↗